Hypothesis 1 - Ligament/Tendon Damage to the Stifle Joint

The patient is an obese large breed active dog, which would predispose Bonnie to traumatic joint disorders.  She likely ruptured one of the tendons or ligaments of the stifle joint while playing in the yard.  The acute onset of the clinical signs is more consistent with a traumatic injury to the joint structure.  The most likely ligament ruptured is the cranial cruciate ligament, due to the presence of the cranial drawer sign.  The absence of the cranial drawer sign without sedation is likely due to the patient being well muscled and resisting manipulation of the painful joint through muscle tone.  The patellar and collateral ligaments of the stifle were palpable and appeared to be intact, so it is unlikely that these ligaments are involved.  The function of the cranial cruciate ligament is to constrain the stifle joint limiting internal rotation and cranial displacement of the tibia relative to the femur.  The most common mechanism of injury to the ligament is rapid rotation of the stifle with the joint in 20-50 degrees of flexion or when the joint is hyper-extended.  This causes internal rotation of the tibia in relation to the femur applying strain to the cranial cruciate ligament.  With internal rotation the caudomedial edge of the lateral femoral condyle rotates putting pressure on the ligament causing partial or complete rupture of the ligament.  With hyperextension, the intercondylar notch compresses and can transect the ligament.  

There is an acute inflammatory response from the tissue damage resulting in capillary hemorrhage and fibrin deposition.  This leads to a cellular response consisting of neutrophils and macrophages that remove the necrotic tissue initiating repair and releasing inflammatory mediators.  These inflammatory mediators, like histamine and bradykinin, cause constriction of the vascular endothelial cells causing the capillaries to become leaky and allowing fluid and more inflammatory cells to enter the site in response to the chemotactic factors released by complement activation.  The inflammatory mediators (biochemical) and the distention of the joint capsule (mechanical) cause activation of the nociceptors leading to pain.

Meniscal injury/damage also needs to be considered which would lead to instability in the joint and could be contributing to the clinical signs.  Primary meniscal damage is rare and is almost always secondary to torn or stretched ligaments.  The damage to the menisci usually results from the cranial drawer allowed by the cranial cruciate rupture.  The medial meniscus is firmly attached to the tibia and as the tibia moves cranially the meniscus is subjected to crushing and shearing forces by the condyle of the femur.